chapter 20 cardiac output

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CARDIAC OUTPUT CARDIAC OUTPUT

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Page 1: Chapter 20   cardiac output

CARDIAC OUTPUTCARDIAC OUTPUT

Page 2: Chapter 20   cardiac output

Cardiac Output, Venous Return Cardiac Output, Venous Return and their Regulationand their Regulation

Cardiac output is controlled to Cardiac output is controlled to maintain the proper amount of flow to maintain the proper amount of flow to tissues and to prevent undue stress tissues and to prevent undue stress on the heart.on the heart.

Page 3: Chapter 20   cardiac output

Cardiac OutputCardiac Output

Generally proportional to body surface Generally proportional to body surface area.area.

Cardiac Index (CI): Approximately 3 Cardiac Index (CI): Approximately 3 liters/min/mliters/min/m22 of body surface area. of body surface area.

CI varies with age, peaking at around 8 CI varies with age, peaking at around 8 years.years.

Page 4: Chapter 20   cardiac output

Frank-Starling LawFrank-Starling Law

What goes into the heart comes out.What goes into the heart comes out.

Increased heart volume stretches muscles Increased heart volume stretches muscles and causes stronger contraction.and causes stronger contraction.

Stretch increases heart rate as well.Stretch increases heart rate as well. Direct effect on sino-atrial nodeDirect effect on sino-atrial node Bainbridge reflex (through the brain)Bainbridge reflex (through the brain)

Page 5: Chapter 20   cardiac output

Cardiac OutputCardiac Output

Depends on venous return, which, in turn, Depends on venous return, which, in turn, depends on the rate of flow to the tissues.depends on the rate of flow to the tissues.

Rate of flow to tissues depends on tissue Rate of flow to tissues depends on tissue needs (i.e. it depends on Total Peripheral needs (i.e. it depends on Total Peripheral Resistance). Therefore, cardiac output is Resistance). Therefore, cardiac output is proportional to the energy requirements of proportional to the energy requirements of the tissues.the tissues.

Page 6: Chapter 20   cardiac output

Limit of Cardiac OutputLimit of Cardiac Output

Normal CO – 5 L/minNormal CO – 5 L/min Plateau – 13 L/minPlateau – 13 L/min Hypereffective heart plateau – 20 L/minHypereffective heart plateau – 20 L/min Hypoeffective heart plateau – 5 L/minHypoeffective heart plateau – 5 L/min

Page 7: Chapter 20   cardiac output

Hypereffective HeartHypereffective Heart

Effected by:Effected by:1.1. Nervous excitation.Nervous excitation.2.2. Cardiac HypertrophyCardiac Hypertrophy

Exercise – Marathon runners may get 30 to Exercise – Marathon runners may get 30 to 40 L/min40 L/min

Aortic Valve StenosisAortic Valve Stenosis

Page 8: Chapter 20   cardiac output

Hypoeffective HeartHypoeffective Heart

Valvular diseaseValvular disease Increased output pressureIncreased output pressure Congential heart diseaseCongential heart disease MyocarditisMyocarditis Cardiac anoxiaCardiac anoxia ToxicityToxicity

Page 9: Chapter 20   cardiac output

Autonomic Nervous SystemAutonomic Nervous System

Causes increased cardiac output when Causes increased cardiac output when vessels become dilated (dinitrophenol).vessels become dilated (dinitrophenol).

Causes venous constriction during Causes venous constriction during exercise.exercise.

Page 10: Chapter 20   cardiac output

Disease States Lowering Total Disease States Lowering Total Peripheral ResistancePeripheral Resistance

Beriberi: insufficient thiamine – tissues Beriberi: insufficient thiamine – tissues starve because they cannot use nutrients.starve because they cannot use nutrients.

AV fistula: e.g. for dialysis.AV fistula: e.g. for dialysis. Hyperthyroidism: Reduced resistance Hyperthyroidism: Reduced resistance

caused by increased metabolismcaused by increased metabolism Anemia (lack of RBCs): effects viscosity Anemia (lack of RBCs): effects viscosity

and transport of Oand transport of O22 to the tissues. to the tissues.

Page 11: Chapter 20   cardiac output

Disease States Lowering Cardiac Disease States Lowering Cardiac OutputOutput

Heart attack, valvular disease, Heart attack, valvular disease, myocarditis, cardiac tamponade, shock.myocarditis, cardiac tamponade, shock.

Shock:Shock: Nutritional deficiency of tissues. Nutritional deficiency of tissues. Decreased venous return caused by:Decreased venous return caused by:

Reduced blood volumeReduced blood volume Venous dilitation (increased circulatory Venous dilitation (increased circulatory

volume)volume) Venous obstructionVenous obstruction

Page 12: Chapter 20   cardiac output

Changes in Intrapleural PressureChanges in Intrapleural Pressure

Generally shift the cardiac Generally shift the cardiac output curve in proportion to output curve in proportion to pressure change (pressure change (breathingbreathing, , Valsalva maneuverValsalva maneuver).).

Cardiac Tamponade (filling of Cardiac Tamponade (filling of pericardial sac with fluid) pericardial sac with fluid) lowers rate of change of CO lowers rate of change of CO with right atrial pressurewith right atrial pressure

HeartPericardial Sac

Rt. Atrial Pressure

CO

tamponade15 L/min

Page 13: Chapter 20   cardiac output

Determinants of Venous ReturnDeterminants of Venous Return

Mean systemic filling pressure

Right Atrial Pressure

Resistance to Flow

Pressure change is slight. Thus, small increase in RA Pressure causes dramatic reduction in venous return. (mean systemic filling pressure).

Page 14: Chapter 20   cardiac output

Normal Venous Return CurveNormal Venous Return Curve

5 L/min

VR (CO)

Rt. Atrial Pressure (mm Hg)

0-4

Mean systemic filling pressure ~ 7 mm Hg

Plateau: collapse of large veins ( => increased resistance)

Venous return with heart and lung removed.

Cardiac Output Curve

Working Cardiac Output

Page 15: Chapter 20   cardiac output

Filling PressureFilling Pressure

Mean Circulatory: The pressure within the Mean Circulatory: The pressure within the circulatory system when all flow is stopped circulatory system when all flow is stopped (e.g. by stopping the heart).(e.g. by stopping the heart).

Mean Systemic: Pressure when flow is Mean Systemic: Pressure when flow is stopped by clamping large veins.stopped by clamping large veins.

The two are close numerically.The two are close numerically.

Page 16: Chapter 20   cardiac output

Venous Return & Cardiac OutputVenous Return & Cardiac Output

Cardiac output increases with atrial Cardiac output increases with atrial pressure.pressure.

Normal atrial pressure is about 0 mm Hg.Normal atrial pressure is about 0 mm Hg. Venous return (with heart and lungs Venous return (with heart and lungs

removed) decreases with atrial pressure.removed) decreases with atrial pressure. Working cardiac output is where venous Working cardiac output is where venous

return curve meets cardiac output curve.return curve meets cardiac output curve.

Page 17: Chapter 20   cardiac output

Compensation for Increased Blood Compensation for Increased Blood VolumeVolume

1.1. Increased CO increases capillary Increased CO increases capillary pressure, sending more fluid to tissues.pressure, sending more fluid to tissues.

2.2. Vein volume increasesVein volume increases3.3. Pooling of blood in the liver and spleenPooling of blood in the liver and spleen4.4. Increased peripheral resistance reduces Increased peripheral resistance reduces

cardiac output.cardiac output.

Page 18: Chapter 20   cardiac output

Effects of Sympathetic StimulationEffects of Sympathetic Stimulation

Increases contractility of the heart.Increases contractility of the heart. Decreases volume by contracting the Decreases volume by contracting the

veins.veins. Increases filling pressureIncreases filling pressure Increases resistanceIncreases resistance

Page 19: Chapter 20   cardiac output

Effects of Sympathetic InhibitionEffects of Sympathetic Inhibition

Shifts CO to the rightShifts CO to the right Shifts venous return Shifts venous return

down and to the leftdown and to the left

- Reduced CO- Reduced CO5 L/min

VR (CO)

Rt. Atrial Pressure (mm Hg)

0-4

Venous return with heart and lung removed.

Page 20: Chapter 20   cardiac output

Effects of AV FistulaEffects of AV Fistula

1.1. Decreased VR resistance.Decreased VR resistance.2.2. Slight increased CO because of reduced Slight increased CO because of reduced

peripheral resistance.peripheral resistance.3.3. After restoration of pressure (sympathetic)After restoration of pressure (sympathetic)4.4. Further CO increase.Further CO increase.5.5. Increased filling pressure.Increased filling pressure.6.6. Decreased kidney output (leads to higher fluid Decreased kidney output (leads to higher fluid

volume and more increase in CO).volume and more increase in CO).7.7. Cardiac hypertrophy (caused by increased Cardiac hypertrophy (caused by increased

workload).workload).

Page 21: Chapter 20   cardiac output

Measurement of COMeasurement of CO

Electromagnetic/ultrasonic (transit time) flow Electromagnetic/ultrasonic (transit time) flow meter.meter.

Oxygen Fick method:Oxygen Fick method: CO = (Rate of O2 absorbed by lungs)CO = (Rate of O2 absorbed by lungs) [O2][O2] lala - [O2] - [O2] rvrv

Indicator dilution method:Indicator dilution method: Inject cold saline (or dye) into RA, measure Inject cold saline (or dye) into RA, measure

temperature (or concentration) in aorta.temperature (or concentration) in aorta.

Page 22: Chapter 20   cardiac output